Transcriptomic analysis of Bacteroides thetaiotaomicron inositol lipid knockout strains
Ontology highlight
ABSTRACT:
ORGANISM(S): Bacteroides thetaiotaomicron
PROVIDER: GSE193734 | GEO | 2022/01/21
REPOSITORIES: GEO
Similar Datasets
Project description:Plants develop mutualistic association with beneficial rhizobacteria. To understand this important phenomenon, early mechanisms for establishing the mutualism are critical. Here we report that active DNA demethylation in plants controls root secretion of myo-inositol, which triggers and further facilitates colonization of the beneficial rhizobacteria Bacillus megaterium strain YC4, thereby allowing for plant growth-promotion. YC4 promotes plant growth but the beneficial effects were lost in the Arabidopsis mutant rdd that is defective in active DNA demethylation. Roots of rdd failed to associate with YC4, meanwhile the level of myo-inositol in root exudates was drastically reduced in rdd. Supplementation of myo-inositol to rdd restored YC4 colonization and plant growth-promotion, while plants with defective myo-inositol monophosphatase also failed in establishing mutualism with YC4. myo-Inositol not only induced chemotaxis of YC4 but also increased YC4 biofilm production, consistent with the transcriptional regulation of YC4 by myo-inositol. In addition, myo-inositol preferentially attracts Bacillus megaterium among the examined bacteria species. Regardless of YC4 inoculation, myo-inositol biosynthesis and catabolism genes are down- and up-regulated, respectively, in rdd compared to wild type plants. The differential expression of myo-inositol homeostasis genes is correlated with local DNA hypermethylation, whereas genetic disruption of the RNA-directed DNA methylation pathway abolished these epigenetic marks and reset the corresponding gene expression patterns, resulting in restored YC4 colonization and plant growth-promotion. Importantly, that active DNA demethylation controls myo-inositol-mediated mutualism between YC4 and plants was also demonstrated in Solanum lycopersicum. Our results uncover an important function of myo-inositol in plant-microbe interactions and its dependence on plant epigenetic regulation.
2022-12-19 | GSE143427 | GEO
Project description:Plants develop mutualistic association with beneficial rhizobacteria. To understand this important phenomenon, early mechanisms for establishing the mutualism are critical. Here we report that active DNA demethylation in plants controls root secretion of myo-inositol, which triggers and further facilitates colonization of the beneficial rhizobacteria Bacillus megaterium strain YC4, thereby allowing for plant growth-promotion. YC4 promotes plant growth but the beneficial effects were lost in the Arabidopsis mutant rdd that is defective in active DNA demethylation. Roots of rdd failed to associate with YC4, meanwhile the level of myo-inositol in root exudates was drastically reduced in rdd. Supplementation of myo-inositol to rdd restored YC4 colonization and plant growth-promotion, while plants with defective myo-inositol monophosphatase also failed in establishing mutualism with YC4. myo-Inositol not only induced chemotaxis of YC4 but also increased YC4 biofilm production, consistent with the transcriptional regulation of YC4 by myo-inositol. In addition, myo-inositol preferentially attracts Bacillus megaterium among the examined bacteria species. Regardless of YC4 inoculation, myo-inositol biosynthesis and catabolism genes are down- and up-regulated, respectively, in rdd compared to wild type plants. The differential expression of myo-inositol homeostasis genes is correlated with local DNA hypermethylation, whereas genetic disruption of the RNA-directed DNA methylation pathway abolished these epigenetic marks and reset the corresponding gene expression patterns, resulting in restored YC4 colonization and plant growth-promotion. Importantly, that active DNA demethylation controls myo-inositol-mediated mutualism between YC4 and plants was also demonstrated in Solanum lycopersicum. Our results uncover an important function of myo-inositol in plant-microbe interactions and its dependence on plant epigenetic regulation.
2022-12-19 | GSE143434 | GEO
Project description:Plants develop mutualistic association with beneficial rhizobacteria. To understand this important phenomenon, early mechanisms for establishing the mutualism are critical. Here we report that active DNA demethylation in plants controls root secretion of myo-inositol, which triggers and further facilitates colonization of the beneficial rhizobacteria Bacillus megaterium strain YC4, thereby allowing for plant growth-promotion. YC4 promotes plant growth but the beneficial effects were lost in the Arabidopsis mutant rdd that is defective in active DNA demethylation. Roots of rdd failed to associate with YC4, meanwhile the level of myo-inositol in root exudates was drastically reduced in rdd. Supplementation of myo-inositol to rdd restored YC4 colonization and plant growth-promotion, while plants with defective myo-inositol monophosphatase also failed in establishing mutualism with YC4. myo-Inositol not only induced chemotaxis of YC4 but also increased YC4 biofilm production, consistent with the transcriptional regulation of YC4 by myo-inositol. In addition, myo-inositol preferentially attracts Bacillus megaterium among the examined bacteria species. Regardless of YC4 inoculation, myo-inositol biosynthesis and catabolism genes are down- and up-regulated, respectively, in rdd compared to wild type plants. The differential expression of myo-inositol homeostasis genes is correlated with local DNA hypermethylation, whereas genetic disruption of the RNA-directed DNA methylation pathway abolished these epigenetic marks and reset the corresponding gene expression patterns, resulting in restored YC4 colonization and plant growth-promotion. Importantly, that active DNA demethylation controls myo-inositol-mediated mutualism between YC4 and plants was also demonstrated in Solanum lycopersicum. Our results uncover an important function of myo-inositol in plant-microbe interactions and its dependence on plant epigenetic regulation.
2022-12-19 | GSE143433 | GEO
Project description:Rhizobium leguminosarum biovar viciae strain 3841 was grown in AMS minimal salts on either glucose ammonia or myo-inositol ammonia and gene expression compared.
2008-12-18 | E-MEXP-1961 | biostudies-arrayexpress
Project description:Samples were obtained as part of a randomized, double blind, placebo-controlled, phase IIb study to determine the effects of myo-inositol in smokers with bronchial dysplasia. Smokers with greater than 1 site of dysplasia identified by autofluorescence bronchoscopy-directed biopsy were randomly assigned to receive oral placebo or myo-inositol, 9 g once/day for two weeks and then twice/day for 6 months. Cytologically normal airway epithelial cells were obtained via bronchoscopy from the right or left mainstem bronchus at baseline and 6 months post-treatment with myo-inositol or placebo from 69 study participants (n=138 samples). The RNA from these samples was isolated and used to prepare libraries for mRNA sequencing. Subjects were classified by response according to their change in dysplasia rate after 6-months. Among subjects with a complete response in the myo-inositol arm, there was a significant decrease in a gene expression signature reflective of PI3K activation.
2016-09-26 | GSE86422 | GEO
Project description:The development of new drugs against tuberculosis and diphtheria is focused on disrupting the biogenesis of the cell wall, the unique architecture of which confers resistance against current therapies. The enzymatic pathways involved in the synthesis of the cell wall by these pathogens are well understood but the underlying regulatory mechanisms are largely unknown. Here, we characterize IpsA, a LacI-type transcriptional regulator conserved among Mycobacteria and Corynebacteria that plays a role in the regulation of cell wall biogenesis. IpsA triggers myo-inositol formation by activating ino1, which encodes inositol phosphate synthase. An IpsA deletion mutant of Corynebacterium glutamicum cultured on glucose displayed significantly impaired growth and presented an elongated cell morphology. Analysis of the polar lipid fraction of the cell wall revealed the absence of inositol-derived lipids. The phenotype of the C. glutamicum M-NM-^TipsA mutant was complemented by homologues from Corynebacterium diphtheriae (dip1969) and Mycobacterium tuberculosis (rv3575), indicating the conserved function of IpsA in the pathogenic species. Additional targets of IpsA with putative functions in cell wall biogenesis were identified and IpsA was shown to bind to a conserved palindromic motif within the corresponding promoter regions. myo-inositol was identified as an effector of IpsA, causing the dissociation of the IpsA-DNA complex in vitro. This characterization of IpsA function and of its regulon sheds light on the complex transcriptional control of cell wall biogenesis in the mycolata taxon and generates novel targets for drug development. To identify genes which were regulated by IpsA (Cg2910), we performed DNA microarray analyses of ATCC 13032 M-NM-^TipsA against wild type. For this purpose RNA was isolated from cells cultivated in CGXII minimal medium with 2% glucose (w v-1) and harvested in the exponential growth phase at an OD600 of 1. Three biological replicates were performed.
2014-01-13 | E-GEOD-50210 | biostudies-arrayexpress
Project description:E. histolytica is believed to be devoid of peroxisomes, like most anaerobic protists. In this work, we provided the first evidence that peroxisomes are present in E. histolytica, although the set of proteins (peroxins) responsible for peroxisome biogenesis was reduced to only seven members (Pex1, Pex6, Pex5, Pex11, Pex14, Pex16, and Pex19). Targeting matrix proteins to peroxisomes is reduced to the PTS1-dependent pathway mediated via the soluble Pex5 receptor, while the PTS2 receptor Pex7 is absent. Immunofluorescence microscopy showed that peroxisomal markers (Pex5, Pex14, Pex16, Pex19) are present in vesicles distinct from mitosomes, the endoplasmic reticulum and the endosome/phagosome system, except Pex11, which has dual localization in peroxisomes and mitosomes. Immunoelectron microscopy revealed that Pex14 localized to vesicles of approximately 90-100 nm in diameter. Proteomic analyses of affinity-purified peroxisomes and in silico PTS1 predictions provided datasets of 655 and 56 peroxisomal candidates, respectively; however, only six proteins were shared by both datasets, including myo-inositol dehydrogenase (myo-IDH). Peroxisomal NAD-dependent myo-IDH appeared to be a dimeric enzyme with high affinity to myo-inositol (Km 0,044 mM) and can utilize also scyllo-inositol, D-glucose and D-xylose as substrates. Phylogenetic analyses revealed that orthologs of myo-IDH with PTS1 are present in E. dispar, E. nutalli and E. moshkovskii but not in E. invadens, and form a monophyletic clade of mostly peroxisomal orthologs with free-living M. balamuthi and P. schiedti. The presence of peroxisomes in E. histolytica and other archamoebae breaks the paradigm of peroxisome absence in anaerobes and provides a new potential target for the development of antiparasitic drugs.
2021-10-29 | PXD026653 | Pride
Project description:The development of new drugs against tuberculosis and diphtheria is focused on disrupting the biogenesis of the cell wall, the unique architecture of which confers resistance against current therapies. The enzymatic pathways involved in the synthesis of the cell wall by these pathogens are well understood but the underlying regulatory mechanisms are largely unknown. Here, we characterize IpsA, a LacI-type transcriptional regulator conserved among Mycobacteria and Corynebacteria that plays a role in the regulation of cell wall biogenesis. IpsA triggers myo-inositol formation by activating ino1, which encodes inositol phosphate synthase. An IpsA deletion mutant of Corynebacterium glutamicum cultured on glucose displayed significantly impaired growth and presented an elongated cell morphology. Analysis of the polar lipid fraction of the cell wall revealed the absence of inositol-derived lipids. The phenotype of the C. glutamicum ΔipsA mutant was complemented by homologues from Corynebacterium diphtheriae (dip1969) and Mycobacterium tuberculosis (rv3575), indicating the conserved function of IpsA in the pathogenic species. Additional targets of IpsA with putative functions in cell wall biogenesis were identified and IpsA was shown to bind to a conserved palindromic motif within the corresponding promoter regions. myo-inositol was identified as an effector of IpsA, causing the dissociation of the IpsA-DNA complex in vitro. This characterization of IpsA function and of its regulon sheds light on the complex transcriptional control of cell wall biogenesis in the mycolata taxon and generates novel targets for drug development.
2014-01-13 | GSE50210 | GEO
Project description:Cryptococcus neoformans is the most common cause of fungal meningitis, with high mortality and morbidity. The reason for the frequent occurrence of Cryptococcus infection in the central nervous system (CNS) is poorly understood. In this study, we find that inositol plays an important role in the transversal of Cryptococcus across the blood-brain barrier (BBB) both in an in vitro human BBB model and in vivo animal models. The inositol stimulation of BBB crossing is dependent upon fungal inositol transporters. The upregulation of genes involved in the inositol catabolism pathway is evident in a microarray analysis. The expression of CPS1, a gene encoding the hyaluronic acid synthase in Cryptococcus, is also upregulated by the inositol treatment. The production of hyaluronic acid increased in cells treated with inositol, which leads to the enhanced binding ability of Cryptococcus cells to the human brain microvascular endothelial cells (HBMECs) constituting the BBB. Overall, our studies provide a mechanism for inositol-dependent Cryptococcus transversal of the BBB, supporting our hypothesis that host inositol utilization by the fungus contributes to Cryptococcus CNS infection.
2012-09-29 | GSE41211 | GEO
Project description:Cryptococcus neoformans is the most common cause of fungal meningitis, with high mortality and morbidity. The reason for the frequent occurrence of Cryptococcus infection in the central nervous system (CNS) is poorly understood. In this study, we find that inositol plays an important role in the transversal of Cryptococcus across the blood-brain barrier (BBB) both in an in vitro human BBB model and in vivo animal models. The inositol stimulation of BBB crossing is dependent upon fungal inositol transporters. The upregulation of genes involved in the inositol catabolism pathway is evident in a microarray analysis. The expression of CPS1, a gene encoding the hyaluronic acid synthase in Cryptococcus, is also upregulated by the inositol treatment. The production of hyaluronic acid increased in cells treated with inositol, which leads to the enhanced binding ability of Cryptococcus cells to the human brain microvascular endothelial cells (HBMECs) constituting the BBB. Overall, our studies provide a mechanism for inositol-dependent Cryptococcus transversal of the BBB, supporting our hypothesis that host inositol utilization by the fungus contributes to Cryptococcus CNS infection. To understand the effect of inositol on gene expression profiles during cell development, microarray experiments were performed to monitor the genes regulated by inositol. H99 overnight culture was washed with dH2O once, and cells were inoculated on SD medium with or without inositol. Cells were collected from SD plates 24 hr post-inoculation, washed with dH2O, and total RNA was purified. Total RNAs were extracted using Trizol Reagents (Invitrogen) and purified using the Qiagen RNeasy cleanup kit (Qiagen). Cy3 and Cy5-labeled cDNA were generated by incorporating amino-allyl-dUTP during reverse transcription of 5 µg of total RNA as described previously and competitively hybridized to a JEC21 whole-genome array generated previously at Washington University in Saint Louis. After hybridization, arrays were scanned with a GenePix 4000B scanner (Axon Instruments, http://www.axon.com) and analyzed by using GenePix Pro version 4.0 and BRB array tools (developed by Richard Simon and Amy Peng Lam at the National Cancer Institute; http://linus.nci.nih.gov/BRB-ArrayTools.html)
2012-09-29 | E-GEOD-41211 | biostudies-arrayexpress